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Inflammation. 2019 Aug 31. doi: 10.1007/s10753-019-01085-z. [Epub ahead of print]

Paeoniflorin Prevents Intestinal Barrier Disruption and Inhibits Lipopolysaccharide (LPS)-Induced Inflammation in Caco-2 Cell Monolayers.

Author information

1
Department of Gastroenterology and Hepatology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
2
Department of Gastroenterology Surgery, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
3
Department of Gastroenterology and Hepatology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. wzykdxhzm@163.com.
4
The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. wzykdxhzm@163.com.
5
The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. wzcgzh@163.com.
6
Department of Pharmacy, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. wzcgzh@163.com.

Abstract

Inflammatory bowel disease (IBD) in humans is closely related to bacterial infection and the disruption of the intestinal barrier. Paeoniflorin (PF), a bioactive compound from Paeonia lactiflora Pallas plants, exerts a potential effect of anti-inflammatory reported in various researches. However, the effect of PF on intestinal barrier function and its related mechanisms has not been identified. Here, we investigate the PF potential anti-inflammatory effect on lipopolysaccharide (LPS)-stimulated human Caco-2 cell monolayers and explore its underlying key molecular mechanism. In this context, PF significantly increased TEER value, decreased intestinal epithelium FITC-dextran flux permeability, and restored the expressions of occludin, ZO-1, and claudin5 in LPS-induced Caco-2 cell. In vitro, treatment of PF significantly inhibited LPS-induced expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), and matrix metalloproteinase-9 (MMP-9). In addition, we found that PF suppressed nuclear factor kappa B (NF-κB) signaling via activating the Nrf2/HO-1 signaling pathways in ILPS-stimulated Caco-2 cells. Our findings indicate that PF has an inhibitory effect on endothelial injury. Our findings suggested that PF has an anti-inflammatory effect in ILPS-stimulated Caco-2 cells, which might be a potential therapeutic agent against IBD and intestinal inflammation.

KEYWORDS:

NF-κB; Nrf2/OH-1; intestinal barrier; paeoniflorin; tight junction protein

PMID:
31473900
DOI:
10.1007/s10753-019-01085-z

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